Variability in sleep disturbance, physical activity and quality of life by level of depressive symptoms in women with Type 2 diabetes.

AIMS: To examine (1) the prevalence of depressive symptoms in women with Type 2 diabetes, (2) the associations between depressive symptoms and the following dependent variables: sleep disturbance; physical activity; physical health-related; and global quality of life, and (3) the potential moderating effects of antidepressants and optimism on the relationship between depressive symptoms and dependent variables. METHODS: Participants in the Women's Health Initiative who had Type 2 diabetes and data on depressive symptoms (N=8895) were included in the analyses. In multivariable linear regression models controlling for sociodemographic, medical and psychosocial covariates, we examined the main effect of depressive symptoms, as well as the interactions between depressive symptoms and antidepressant use, and between depressive symptoms and optimism, on sleep disturbance, physical activity, physical health-related quality of life; and global quality of life. RESULTS: In all, 16% of women with Type 2 diabetes reported elevated depressive symptoms. In multivariable analyses, women with depressive symptoms had greater sleep disturbance (P<0.0001) and lower global quality of life (P<.0001). We found evidence of significant statistical interaction in the models for quality-of-life outcomes: the increased risk of poor physical health-related quality of life associated with antidepressant use was stronger in women without vs with depressive symptoms, and the association between greater optimism and higher global quality of life was stronger in women with vs without depressive symptoms. CONCLUSIONS: To improve health behaviours and quality of life in women with Type 2 diabetes, sociodemographic and medical characteristics may identify at-risk populations, while psychosocial factors including depression and optimism may be important targets for non-pharmacological intervention.

Weight gain in infancy and early childhood is associated with school age body mass index but not intelligence and blood pressure in very low birth weight children.

Rates of weight gain in infancy and early childhood can influence later neurocognitive, metabolic and cardiovascular health. We studied the relationship of weight gain during infancy and early childhood to intelligence quotient (IQ), blood pressure (BP) and body mass index (BMI) at age 9 in children born with very low birth weight (VLBW). Sixty-five children born prematurely with VLBW were followed longitudinally and at 9 years IQ, BP and BMI were measured. The mean weight z-scores at birth, neonatal intensive care discharge, 1 year corrected for prematurity, 5 and 9 years were -0.17, -2.09, -1.3, -0.68 and 0.06, respectively. Weight gain during infancy (discharge to 1 year corrected for prematurity) and early childhood (1 year corrected age to 5 years) was expressed as rate of change in weight, rate of change in weight z-score and interval change in weight z-score. In multiple regression analyses that adjusted for race, gender, maternal education, antenatal steroids, birth weight z-score, major intracranial lesions on ultrasound and chronic lung disease, rates of weight gain in infancy and early childhood were predictive of BMI z-score at 9 years, regression coefficients (95% confidence intervals); 0.19 (0.02, 0.36) and 0.37 (0.11, 0.63), respectively, expressed as change in BMI z-score per 10 g/week weight increase. Rates of weight gain were not predictive of systolic BP z-score, Verbal IQ or Performance IQ. In VLBW infants, more rapid weight gain during infancy, and especially early childhood, is associated with higher BMI at school age.

Development and validation of the Dermatomyositis Skin Severity Index.

BACKGROUND: Dermatomyositis is an autoimmune inflammatory muscle disease with characteristic cutaneous findings of heliotrope eruption, Gottron's papules and a photodistributed eruption with poikiloderma. OBJECTIVES: To develop and validate a tool to assist with objective assessment of the skin disease of dermatomyositis. METHODS: A skin severity index was developed; content validity was evaluated by a panel of experts, and construct validity was assessed by convergence with other measures of disease severity including physician's global assessment of disease, specific skin disease changes (ulceration, poikiloderma and pruritus), and quality of life. Test and retest reliability and interobserver reproducibility were determined. RESULTS: In total, 98 subjects were enrolled. The Dermatomyositis Skin Severity Index (DSSI) showed significant correlation to the physician's global assessment, assessments of poikiloderma and self-assessment of pruritus. Inter-rater reliability showed strong correlations from 0.73 to 1. Test-retest (intrarater reliability) was completed on 33 subjects, and showed correlations above 0.75. The ability of this tool to detect clinical changes with treatment has not been fully evaluated. CONCLUSIONS: The DSSI is a valid and reliable measure of skin disease severity in dermatomyositis and can be used in future clinical trials as an assessment tool.

A genome-wide linkage scan for iron phenotype quantitative trait loci: the HEIRS Family Study.

Iron overload phenotypes in persons with and without hemochromatosis are variable. To investigate this further, probands with hemochromatosis or evidence of elevated iron stores and their family members were recruited for a genome-wide linkage scan to identify potential quantitative trait loci (QTL) that contribute to variation in transferrin saturation (TS), unsaturated iron-binding capacity (UIBC), and serum ferritin (SF). Genotyping utilized 402 microsatellite markers with average spacing of 9 cM. A total of 943 individuals, 64% Caucasian, were evaluated from 174 families. After adjusting for age, gender, and race/ethnicity, there was evidence for linkage of UIBC to chromosome 4q logarithm of the odds (LOD) = 2.08, p = 0.001) and of UIBC (LOD = 9.52), TS (LOD = 4.78), and SF (LOD = 2.75) to the chromosome 6p region containing HFE (each p < 0.0001). After adjustments for HFE genotype and other covariates, there was evidence of linkage of SF to chromosome 16p (LOD = 2.63, p = 0.0007) and of UIBC to chromosome 5q (LOD = 2.12, p = 0.002) and to chromosome 17q (LOD = 2.19, p = 0.002). We conclude that these regions should be considered for fine mapping studies to identify QTL that contribute to variation in SF and UIBC.